This paper appeared in Learning and Individual Differences, 10, 179-191 (1999) Does the study of autism justify minimalist innate modularity? Simon Baron-Cohen Departments of Experimental Psychology and Psychiatry University of Cambridge Downing St, Cambridge, CB2 3EB, UK 1 Acknowledgements: The author was supported by the Medical Research Council and the Wellcome Trust during the preparation of this work. 2 Abstract Innate modularity is the big question for cognitive neuroscience. One proposal is that a ‘theory of mind’ is a species-specific (human) example of an innate module. The evidence from the genetic, neurodevelopmental, psychiatric condition of autism is considered, to examine if the innate modularity claim is justified. At the opposite extreme, explanations of autism in terms of deficits in a general learning mechanism are considered. It is concluded that both of these extreme positions may be untenable, and instead there may be some justification for an intermediate model of social perception: minimalist innate modularity. 3 Introduction The study of autism has been the battleground for modularity and anti-modularity theorists. On the side of modularity are scientists who view the theory of mind deficit in autism as evidence for some form of modularity (Baron-Cohen, 1995; Happe & Frith, 1996; Leslie, 1991). On the side of anti-modularity are those who only recognise the brain as a general learning mechanism such as (Mackintosh, McLaren, Plaisted); or those theorists such as Russell (Russell, 1997a) and Pennington (Pennington et al., in press), who view the theory of mind deficit in autism as part of a broader deficit in higher order cognitive processes such as executive function (Shallice, 1988). In some senses, this battle is simply an example of the wider battle in cognitive neuroscience, since ultimately everyone in the larger field needs to take a position on whether modules exist, or what if anything is innate in the cognitive system. Although this article focuses on the arguments in relation to theory of mind being modular (using evidence from autism), readers can easily apply these arguments in relation to language (using evidence from language disorder) or in relation to other domains. First, we introduce autism and the theory of mind hypothesis. Background: Autism and the theory of mind hypothesis Autism is considered to be the most severe of the childhood neuropsychiatric conditions. It is diagnosed on the basis of abnormal development of social behaviour, communication, and imagination, often in the presence of marked obsessional, repetitive, 4 or ritualistic behaviour (APA, 1994). The theory of mind hypothesis states that children with autism are impaired in the development of the ability to appreciate their own and other people's mental states - such as their beliefs, desires, intentions, knowledge, pretence, and perception - and the links between mental states and action. Because of the importance of a theory of mind (henceforth ToM) in normal social interaction, social understanding, imagination and communication, a deficit in the development of a ToM is a powerful way to explain abnormalities in these areas in autism. First-order theory of mind tests involve inferring what one person thinks, knows, intends, desires, etc. The majority of children with autism are at chance on such tests. 21 tests are summarized highly concisely in Table 1. By way of illustration, one of these is described in more detail: the “seeing leads to knowing” test. This was originally developed by Chris Pratt and Peter Bryant (Pratt & Bryant, 1990). They presented a story (using dolls) to 3-4 year old normally developing children. The story is short and illustrated in Figure 1. Thus, Sally and Anne are introduced, and the subject is told that Sally touches the box, whilst Anne looks inside the box. The subject is then asked “Which one knows what’s inside the box?” Pratt and Bryant found that normal 3-4 year old children could correctly identify the character who knows what’s in the box (in this example, Anne). If you ask the normal child of this age why they chose Anne, they can say, “Well, she knows, because she looked.” In passing this test, children are thus demonstrating their understanding of a corner-stone of their theory of mind, namely the principle that seeing-leads-to-knowing. When this same test was given to a group of children with autism, and a second group of children without 5 autism but with mental handicap1, both of whom had a mental age (MA) above 4 years old, the group with mental handicap passed the test in line with their MA, whereas the children with autism were significantly impaired on the task. Indeed, they were as likely to choose Anne as they were to choose Sally, suggesting they did not grasp this principle, and were mostly guessing. Because this deficit occurred in the presence of sufficient MA, it is taken as evidence of a specific ToM deficit. Most of the other results in Table 1 reveal a similar pattern of autism-specific, ToM-specific deficit. insert Table 1 and Figure 1 here This list of experiments provides strong converging evidence for there being a theory of mind deficit in autism. For this reason, autism has been conceptualized as involving “mindblindness” to varying degrees (Baron-Cohen, 1990; Baron-Cohen, 1995). Brothers’ social brain theory In an important article in 1990, Leslie Brothers suggested that social intelligence should be distinguished from other kinds of intelligence, and that social intelligence might have its own dedicated neural circuitry (involving the amygdala, orbito-frontal cortex (OFC), and superior temporal sulcus (STS). Evidence for her proposal included the existence of brain-damaged patients who seemed to show selective impairments in social judgement, 1 Here, we use the term ‘mental handicap’ to refer to children with general developmental delay and below average IQ. In the UK the term ‘learning difficulties’ is preferred, but in the USA this latter term has a different meaning. Hence the use of the former term here. 6 lesion studies of the non-human animal brain selectively affecting social behaviour, and single cell recording studies identifying cells that fire only in response to social stimuli (such as faces and hands). She referred to these three neural regions as comprising the “social brain”. Leslie’s modularity contention Alan Leslie, independently of Brothers, suggested that there may be a particular part of the brain which in the normal case is specifically responsible for understanding mental states, and which is impaired in autism. He proposed this may be modular, and he coined the term ‘theory of mind mechanism’ (ToMM) as shorthand for this (Leslie, 1991; Leslie & Roth, 1993; Leslie, 1987). ToMM may be part of the social brain (Baron-Cohen, 1995). Note that the term ‘module’ in this theory is not necessarily defined using all of Fodor’s 9 criteria (Fodor, 1983); rather, varieties of modularity are conceptualized. But critically for Leslie and others, at a minimum such modules are in part innate, and computationally dedicated or specific to a particular class of input. Leslie suggests the function of the theory of mind mechanism is to represent information in a data-structure of the following form: [Agent-Attitude-"Proposition"] - eg: [Fred-thinks-"the safe is behind the Picasso"]. Such a proposal is sufficient to allow representation of the full range of mental states, in the Attitude slot. Such representations allow one to make sense of why Fred, a burglar in this example, is seen as lifting the Picasso painting off the wall, or would enable one to predict where Fred would look in the house. 7 Leslie’s computational analysis has been widely accepted, but the innate modularity claim is more controversial (Carruthers, 1996; Russell, 1997b). Anti-modularity arguments in relation to theory of mind Arguments against the ToM deficit in autism being proof of modularity are as follows: 1. Circularity - one cannot use autism as both the proof of a ToM deficit and proof this being modular in the normal case. One needs independent lines of evidence to prove or disprove the modularity thesis. For example, finding a universal pattern of ontogenesis to the development of a theory of mind, in normal development, or double dissociations between theory of mind and executive function in neurological patients, would bolster the modularity position. In fact, there is some evidence for universal ontogenetic similarity (Avis & Harris, 1991). Double dissociation evidence is also available (reviewed later). 2. Profligacy - Whilst it may seem parsimonious to explain all the cognitive evidence showing deficits by positing a ToM module, can this be justified given how complex such a ToM module would have to be? For example, it would have to store the complete set of mental state concepts in advance. Anti-nativists should rightly be concerned that too much may be being built in at the innate level, with insufficient support for this. 8 3. Ignoring the role of learning - we know normal infants and toddlers spend many long hours engaged in social interaction. Is this just for reasons of attachment and vocabulary learning, or might this be necessary experience for acquiring a ToM too? If so, might ToM (modular or otherwise) be acquired rather than innate, or (more likely) an interaction of both innate and environmental factors? The fact that blind children may be delayed in the theory of mind development (Brown, Hobson, Lee & Stevenson, 1997), or that there are birth-order effects in this domain (Perner, Ruffman & Leekam, 1994) suggests environmental input is important. Alternative modularity theories 1. Baron-Cohen’s minimalist innate modularity theory Leslie’s claim is not the only modular theory, and we need to consider the alternatives. For example, (Baron-Cohen, 1994) suggests lower level perceptual mechanisms extract relevant social information, which provide critical inputs to developing a ToM. These mechanisms include an Eye Direction Detector (or EDD) which grabs the infant’s attention to the eye region of faces and thus provides opportunities for the infant to learn the significance of gaze as a clue to a person’s mental states; an Intentionality Detector (or ID) which grabs the infant’s attention to animate actions, providing opportunities for the infant to learn about goal-directedness; and a Shared Attention Mechanism (or SAM), which takes inputs from the previous two mechanisms to enable the infant to work out if s/he and another person are attending to the same thing, thus ensuring that shared foci or 9 common topics are a central experience for the developing infant. ToMM, in this model, is conceived of either being a more mature development of SAM, or is triggered by SAM. We might label Baron-Cohen’s model a minimalist innate modularity theory. Rather than having to postulate ToMM coming fully prepackaged as an innate module, this minimalist alternative specifies less that is innate - but still specfies some innate social-information mechanisms. 2. Johnson and Morton’s even more minimalist innate modularity theory However, once one considers more minimalist versions of the innate modularity theory, one is forced to take seriously even more minimalist possibilities. Thus, Morton and Johnson (Morton & Johnson, 1991) do not even go as far as suggesting the existence of innate mechanisms as complex or as specfic as EDD, ID, and SAM. Instead, they simply postulate a mechanism called CONSPEC, which grabs the infant’s attention to look at face-like stimuli. A second innate mechanism (CONLERN) then steers the infant attentional system to learn all about faces. On this argument, our strong intuition that looking at eyes is innate does not reflect an EDD, but simply reflects that eyes are parts of the face that move alot, and CONLERN ensures we track such changeable social stimuli in order to learn what they predict. On their model, if we have modules like EDD, SAM, and ToMM, these are acquired, not innate, modules. Interim summary 10 If we pause at this point, we can summarize the debate so far: Leslie’s proposal of a rich innate module (ToMM) may be simply the end result of a set of simpler innate modules (EDD, ID, and SAM:(Baron-Cohen, 1995)); but that even these may be the end result of yet simpler innate modules (CONSPEC and CONLERN:(Morton & Johnson, 1991)). Finally, anti-nativists would argue that all of the domains of knowledge we have discussed so far (knowledge about eyes, intentional actions, theory of mind) may be modular in the sense of being domains of expertise in the normal system, but these may just as plausibly be acquired modules, not innate ones (Karmiloff-Smith, 1992). 11 So why not go the whole hog? Why not say there’s no modularity at all? Those readers who are still engaged by this point might reasonably ask: why stop this train of argument at an innate CONSPEC or CONLERN? Instead, one could postulate that even these may be mere endpoints arising out of a general learning mechanism that is working on input from this particular planet. That is, maybe there is nothing innate in cognition, and that apparent similarities in development within and across cultures simply reflect that we are all taking as input into a general learning mechanism information about the same sort of environment. Our environment, in every culture, is populated by people with faces, eyes, actions, etc., so unmysteriously, this is what we end up learning about. This view is certainly alive and well among the learning theorists (Mackintosh, McLaren, Plaisted). If one really wanted to strive for parsimony, surely the liquidized soup model of the mind (no innate structure, no lumpy bits) is surely the most attractive option? Not quite. For one thing, the no-innate modules view has a hard time accounting for cases of pure social deficit. Why should someone with good general intelligence (a good general learning mechanism?) excel in the domain of physics, or maths, or engineering, and yet have difficulties in the social domain? Cases of Asperger Syndrome (Asperger, 1944) may fit this characterization. Further problems for the General Learning Mechanism theory 12 The general learning mechanism theorist might also have difficulty accounting for the following kinds of neurological patients: (1) Patients with severe SLI (specific language impairment) but with intact ToM suggesting the potential independence of language and ToM. Van der Lely has reported one such patient (Van der Lely, 1997). (2) Patients with impaired executive function (EF) but intact ToM suggesting the potential independence of EF and ToM. Some patients with Tourette Syndrome meet this criteria (Baron-Cohen, Robertson & Moriarty, 1994). (3) Patients with impaired ToM but intact EF. (Baron-Cohen, Stone, Wheelwright & Rutherford, 1998) describe a single case of a Cambridge University academic with Asperger Syndrome who had exactly this profile. (4) Patients with low IQ but intact ToM. Patients with Williams Syndrome can show this profile (Karmiloff-Smith, Grant, Bellugi & Baron-Cohen, 1995; Tager-Flusberg, Boshart & Baron-Cohen, in press). (5) Patients with acquired neurological lesions who lose only mentalizing skills. Some patients with amygdala or orbitofrontal cortex lesions have been reported to show this pattern (Stone, Baron-Cohen, Young & Calder, 1998). 13 The above cases strongly suggest modularity of ToM, but are silent on the question of whether this is innate or acquired modularity. Testing for minimalist innate modularity in the social domain How might this debate be resolved through experimental investigation? The following sorts of evidence would all disprove the general learning mechanism view of the mind a) If neonates prefer faces. This has in fact been demonstrated over 40 years ago, and replicated many times (Johnson & Morton, 1991). This stongly implies an innate attentional bias towards social information. b) If faces are processed by specific brain regions. This could be acquired modularity, but if the neural specificity was also found in neonates, this again implies innate neurocognitive structure to the mind, towards social information, along the lines suggested by Brothers (Brothers, 1990). c) If neonates with autism show no face preference. This has never been tested, and would be difficult to do so until we have a biological marker for identifying neonates who will go on to develop autism. But such a finding would refute a general learning mechanism account. 14 d) If there was strong heritability for ToM/social intelligence2. Again, this has not yet been tested, but if confirmed this would imply that the ToM deficit in autism occurs for genetic reasons. This is not implausbile, since autism appears to be strongly heritable (Bailey et al., 1995; Bolton & Rutter, 1990; Le Couteur et al., 1996). The idea that the development of theory of mind is under genetic/biological control in the normal case is consistent with evidence from cross-cultural studies: Normally developing children from markedly different cultures seem to pass tests of theory of mind at roughly the same ages (Avis & Harris, 1991). e) If there was neural specificity to ToM. This could reflect acquired rather than innate specificity, unless such localization was demonstrable in infants. Quite which part of the brain might subserve ToM is not yet clear, though from Brothers’ proposal and related work, candidate regions include the following: (i) right orbito-frontal cortex, which is active when subjects are thinking about mental state terms during functional imaging using SPECT (Baron-Cohen et al., 1994); (ii) left medial frontal cortex, which is active when subjects are drawing inferences about thoughts whilst being PET scanned (Fletcher et al., 1995; Goel, Grafman, Sadato & Hallett, 1995). The first PET study to look at adults with autism/Asperger Syndrome during a ToM task shows that such patients do not show the same patterns of neural activation when thinking about other minds (Happe et al., 1996). 2 Here, the terms ToM and social intelligence are being used coterminously. 15 (iii) Other candidate regions include the amygdala (Baron-Cohen and Ring, 1994). Ongoing studies suggest adult patients with acquired amygdala lesions have difficulties with advanced (or adult level) theory of mind tasks (Stone et al., 1998), and a recent fMRI study of ToM using the Eyes Task found that whilst normal controls used areas of the fronto-temporal cortex and the amygdala, high functioning adults with autism or AS do not activate the amygdala during this task (Baron-Cohen et al., submitted). (iv) Finally, the demonstration of a joint attention (gaze-monitoring) deficit in autism, and the role that the superior temporal sulcus in the monkey brain plays in the monitoring of gaze-direction (Perrett et al., 1985) has led to the idea that the superior temporal sulcus may be involved in the development of a theory of mind (Baron-Cohen & Ring, 1994). Conclusions The available data allow us to interpret the theory of mind deficit in autism as strong evidence for modularity of social intelligence, but may not justify a rich innate module such as Leslie’s ToMM. Rather, a ToMM may be the result of both innate and acquired factors in development. When seen early in development, young children with autism do not show joint attention or normal preferential attention to faces and eyes (Baron-Cohen et al., 1996; Charman, Swettenham, Baron-Cohen, Cox & Baird, 1997), which is at least consistent with a minimalist innate modularity theory (Baron-Cohen, 1995) involving lower-level social perception mechanisms. 16 There is an outside chance that a general learning mechanism theory could be rescued by arguing that the normal neonatal preference for attending to faces and eyes is not a sign of a social-cognitive module but simply a reflection of the general learning mechanism preferring complexity (faces being arguably more complex stimuli than inanimate objects). This would seem to be empirically testable in principle, by matching stimuli for complexity. Johnson and Morton have, in fact, attempted to control for complexity by matching their stimuli (faces and non-faces) for spatial frequency. It may be that there are other aspects of stimulus complexity that need to be controlled. Either way, the minimalist innate modularity theorist would predict that an infant with autism may attend to equally complex stimuli from the non-social domain but simply not attend preferentially to the social stmuli. The anti-modular, general leaning mechanism theorist in contrast would predict that infants with autism would be less interested in any kind of complex stimuli, whether social or non-social. Such tests are for the future. 17 Table 1: 21 Tests of theory of mind in people with autism 1. the mental-physical distinction (Baron-Cohen, 1989b); 2. understanding of the functions of the mind (ibid); 3. the appearance-reality distinction (ibid), 4. first-order false belief tasks, (Baron-Cohen, Leslie & Frith, 1985; Baron-Cohen, Leslie & Frith, 1986; Leekam & Perner, 1991; Perner, Frith, Leslie & Leekam, 1989; Reed & Peterson, 1990; Swettenham, Baron-Cohen, Gomez & Walsh, 1996) (Swettenham, 1996); 5. "seeing leads to knowing" tests (Baron-Cohen & Goodhart, 1994; Leslie & Frith, 1988); 6. tests of recognizing mental state words (like "think", "know", and "imagine") in a wordlist (Baron-Cohen et al., 1994). 7. Tests of production of the same range of mental state words in their spontaneous speech (Baron-Cohen et al., 1986; Tager-Flusberg, 1992); 8. Tests of the production of spontaneous pretend play (Baron-Cohen, 1987; Lewis & Boucher, 1988; Wing & Gould, 1979) (Ungerer et al, 1981); 9. Tests of understanding more complex causes of emotion (such as beliefs) (BaronCohen, 1991a; Baron-Cohen, Spitz & Cross, 1993). 10. Tests of recognizing the eye-region of the face as indicating when a person is thinking and what a person might want (Baron-Cohen, Campbell, Karmiloff-Smith, Grant & Walker, 1995; Baron-Cohen & Cross, 1992); 18 11. Tests of being able to monitor their own intentions (Phillips, Baron-Cohen & Rutter, in press); 12. Tests of deception (Baron-Cohen, 1992; Sodian & Frith, 1992; Yirmiya, SolomonicaLevi & Shulman, 1996); 13. Tests of understanding metaphor, sarcasm, and irony; 14. Tests of pragmatics in their speech (Baron-Cohen, 1988; Tager-Flusberg, 1993); 15.Tests of recognition of violations of pragmatic rules (Surian, Baron-Cohen & Van der Lely, 1996); 16. Tests of imagination (Scott & Baron-Cohen, 1996). 17. Performance on ToM tasks by children with autism has been found to correlate with real-life social skills, as measured by a modified version of the Vineland Adaptive Behaviour Scale (Frith, Happe & Siddons, 1994). 18. A small minority of children or adults with autism pass first-order false belief tests. However, these individuals often fail second-order false belief tests (Baron-Cohen, 1989c).This suggests there can be a specific developmental delay in theory of mind at a number of different points. 19. Some individuals with autism who are very high functioning (in terms of IQ and language level), and who are usually adults, may pass even second-order (Bowler, 1992; Happe, 1993; Ozonoff, Pennington & Rogers, 1991). Those who can pass second-order tests however may have difficulties in understanding stories in which characters are motivated by complex mental states such as bluff and double bluff (Happe, 1994). 20.Such able subjects have difficulties in decoding complex mental states from the expression in the eye-region of the face (Baron-Cohen, Jolliffe, Mortimore & Robertson, 19 1997; Baron-Cohen, Wheelwright & Jolliffe, 1997). Again, this suggests that the mindreading deficit may only be detectable in such high-level, older subjects using sensitive, age-appropriate tests. 21. Parents of children with AS, at least one of whom presumably carries the genes for AS, also show difficulties in attributing mental states when just the eye-region of the face is available (Baron-Cohen & Hammer, 1997). 20 References APA. (1994). DSM-IV Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Washington DC: American Psychiatric Association. Asperger, H. (1944). Die "Autistischen Psychopathen" im Kindesalter. Archiv fur Psychiatrie und Nervenkrankheiten, 117, 76-136. Avis, J., & Harris, P. (1991). Belief-desire reasoning among Baka children: evidence for a universal conception of mind. Child Development, 62, 460-467. Bailey, T., Le Couteur, A., Gottesman, I., Bolton, P., Simonoff, E., Yuzda, E., & Rutter, M. (1995). Autism as a strongly genetic disorder: evidence from a British twin study. Psychological Medicine, 25, 63-77. Baron-Cohen, S. (1987). Autism and symbolic play. British Journal of Developmental Psychology, 5, 139-148. Baron-Cohen, S. (1988). Social and pragmatic deficits in autism: cognitive or affective? Journal of Autism and Developmental Disorders, 18, 379-402. Baron-Cohen, S. (1989b). The autistic child's theory of mind: a case of specific developmental delay. Journal of Child Psychology and Psychiatry, 30, 285-298. Baron-Cohen, S. (1989c). Perceptual role-taking and protodeclarative pointing in autism. British Journal of Developmental Psychology., 7, 113-127. Baron-Cohen, S. (1990). Autism: a specific cognitive disorder of "mindblindness". International Review of Psychiatry, 2, 79-88. Baron-Cohen, S. (1991a). Do people with autism understand what causes emotion? Child Development, 62, 385-395. Baron-Cohen, S. (1992). Out of sight or out of mind: another look at deception in autism. Journal of Child Psychology and Psychiatry, 33, 1141-1155. Baron-Cohen, S. (1994). How to build a baby that can read minds: Cognitive mechanisms in mindreading. Cahiers de Psychologie Cognitive/ Current Psychology of Cognition, 13, 513-552. Baron-Cohen, S. (1995). Mindblindness: an essay on autism and theory of mind.: MIT Press/Bradford Books. Baron-Cohen, S., Campbell, R., Karmiloff-Smith, A., Grant, J., & Walker, J. (1995). Are children with autism blind to the mentalistic significance of the eyes? British Journal of Developmental Psychology, 13, 379-398. Baron-Cohen, S., Cox, A., Baird, G., Swettenham, J., Drew, A., Nightingale, N., Morgan, K., & Charman, T. (1996). Psychological markers of autism at 18 months of age in a large population. British Journal of Psychiatry, 168, 158-163. Baron-Cohen, S., & Cross, P. (1992). Reading the eyes: evidence for the role of perception in the development of a theory of mind. Mind and Language, 6, 173-186. Baron-Cohen, S., & Goodhart, F. (1994). The "seeing leads to knowing" deficit in autism: the Pratt and Bryant probe. British Journal of Developmental Psychology, 12, 397-402. Baron-Cohen, S., & Hammer, J. (1997). Parents of children with Asperger Syndrome: what is the cognitive phenotype? Journal of Cognitive Neuroscience, 9, 548554. 21 Baron-Cohen, S., Jolliffe, T., Mortimore, C., & Robertson, M. (1997). Another advanced test of theory of mind: evidence from very high functioning adults with autism or Asperger Syndrome. Journal of Child Psychology and Psychiatry, 38, 813-822. Baron-Cohen, S., Leslie, A. M., & Frith, U. (1985). Does the autistic child have a 'theory of mind'? Cognition, 21, 37-46. Baron-Cohen, S., Leslie, A. M., & Frith, U. (1986). Mechanical, behavioural and Intentional understanding of picture stories in autistic children. British Journal of Developmental Psychology, 4, 113-125. Baron-Cohen, S., & Ring, H. (1994). A model of the mindreading system:neuropsychological and neurobiological perspectives. In P. Mitchell & C. Lewis (Eds.), Origins of an understanding of mind, : Lawrence Erlbaum Associates. Baron-Cohen, S., Ring, H., Moriarty, J., Shmitz, P., Costa, D., & Ell, P. (1994). Recognition of mental state terms: a clinical study of autism, and a functional neuroimaging study of normal adults. British Journal of Psychiatry, 165, 640-649. Baron-Cohen, S., Ring, H., Williams, S., Wheelwright, S., Bullamore, E., Brammer, M., & Andrew, C. (submitted). Social intelligence: the role of the amygdala. . Baron-Cohen, S., Robertson, M., & Moriarty, J. (1994). The development of the will: a neuropsychological analysis of Gilles de la Tourette's Syndrome. In D. Cicchetti & S. Toth (Eds.), The Self and its Dysfunction: Proceedings of the 4th Rochester Symposium, : University of Rochester Press. Baron-Cohen, S., Spitz, A., & Cross, P. (1993). Can children with autism recognize surprise? Cognition and Emotion, 7, 507-516. Baron-Cohen, S., Stone, V., Wheelwright, S., & Rutherford, M. (1998). A pure case of social intelligence deficit : University of Cambridge. Baron-Cohen, S., Wheelwright, S., & Jolliffe, T. (1997). Is there a "language of the eyes"? Evidence from normal adults and adults with autism or asperger syndrome. Visual Cognition, 4, 311-331. Bolton, P., & Rutter, M. (1990). Genetic influences in autism. International Review of Psychiatry, 2, 67-80. Bowler, D. M. (1992). Theory of Mind in Asperger Syndrome. Journal of Child Psychology and Psychiatry. Brothers, L. (1990). The social brain: a project for integrating primate behaviour and neurophysiology in a new domain. Concepts in Neuroscience, 1, 27-51. Brown, R., Hobson, P., Lee, A., & Stevenson, J. (1997). Are there 'autistic-like' features in congenitally blind children? Journal of Child Psychology and Psychiatry, 38, 693-704. Carruthers, P. (1996). Autism as mindblindness: An elaboration and partial defense. In P. Carruthers (Ed.), Theories of theories of mind, . Cambridge: Cambridge University Press. Charman, T., Swettenham, J., Baron-Cohen, S., Cox, A., & Baird, G. (1997). Infants with autism: an investigation of empathy, joint attention, pretend play, and imitation. Developmental Psychology, 33, 781-789. Fletcher, P. C., Happe, F., Frith, U., Baker, S. C., Dolan, R. J., Frackowiak, R. S. J., & Frith, C. D. (1995). Other minds in the brain: a functional imaging study of "theory of mind" in story comprehension. Cognition, 57, 109-128. Fodor, J. (1983). The modularity of mind: MIT/Bradford Books. 22 Frith, U., Happe, F., & Siddons, F. (1994). Autism and theory of mind in everyday life. Social Development, 3, 108-124. Goel, V., Grafman, J., Sadato, N., & Hallett, M. (1995). Modelling other minds. Neuroreport, 6, 1741-1746. Happe, F. (1993). Communicative competence and theory of mind in autism: A test of Relevance Theory. Cognition, 48, 101-119. Happe, F. (1994). An advanced test of theory of mind: Understanding of story characters' thoughts and feelings by able autistic, mentally handicapped, and normal children and adults. Journal of Autism and Development Disorders, 24, 129-154. Happe, F., Ehlers, S., Fletcher, P., Frith, U., Johansson, M., Gillberg, C., Dolan, R., Frackowiak, R., & Frith, C. (1996). "Theory of mind" in the brain. Evidence from a PET scan study of Asperger Syndrome. NeuroReport, 8, 197-201. Happe, F., & Frith, U. (1996). The neuropsychology of autism. Brain, 119, 13771400. Johnson, M., & Morton, J. (1991). Biology and cognitive development: the case of face recognition. Oxford: Blackwell. Karmiloff-Smith, A. (1992). Beyond modularity: MIT Press/Bradford Books. Karmiloff-Smith, A., Grant, J., Bellugi, U., & Baron-Cohen, S. (1995). Is there a social module? Language, face-processing and theory of mind in William's Syndromeand autism, in press. Journal of Cognitive Neuroscience, 7, 196-208. Le Couteur, A., Bailey, A., Goode, S., Pickles, A., Robertson, S., Gottesman, I., & Rutter, M. (1996). A broader phenotype of autism: the clinical spectrum in twins. Journal of Child Psychology and Psychiatry, 37, 785-801. Leekam, S., & Perner, J. (1991). Does the autistic child have a metarepresentational deficit? Cognition, 40, 203-218. Leslie, A. (1991). The theory of mind impairment in autism: evidence for a modular mechanism of development? In A. Whiten (Ed.), Natural theories of mind, (pp. 63-78). Oxford : Basil Blackwell. Leslie, A., & Roth, D. (1993). What can autism teach us about metarepresentation? In S. Baron-Cohen, H. Tager-Flusberg, & D. Cohen (Eds.), Understanding other minds: perspectives from autism, . Oxford: Oxford Medical Publications. Leslie, A. M. (1987). Pretence and representation: the origins of "theory of mind". Psychological Review, 94, 412-426. Leslie, A. M., & Frith, U. (1988). Autistic children's understanding of seeing, knowing, and believing. British Journal of Developmental Psychology, 6, 315-324. Lewis, V., & Boucher, J. (1988). Spontaneous, instructed and elicited play in relatively able autistic children . British Journal of Developmental Psychology, 6, 325339. Morton, J., & Johnson, M. (1991). CONSPEC and CONLERN: a two-process theory of infant face-recognition. Psychological Review, 98, 164-181. Ozonoff, S., Pennington, B., & Rogers, S. (1991). Executive function deficits in high-functioning autistic children: relationship to theory of mind. Journal of Child Psychology and Psychiatry, 32, 1081-1106. 23 Pennington, B., Rogers, S., Bennetto, L., Griffith, E., Reed, D., & Shyu, V. (in press). Validity Test of the Executive Dysfunction Hypothesis of Autism. In J. Russell (Ed.), Executive Functioning in Autism, . Oxford: Oxford University Press. Perner, J., Frith, U., Leslie, A. M., & Leekam, S. (1989). Exploration of the autistic child's theory of mind: knowledge, belief, and communication. Child Development, 60, 689-700. Perner, J., Ruffman, T., & Leekam, S. (1994). Theory of mind is contagious: You catch it from your sibs. Child Development, 65, 1228-1238. Perrett, D., Smith, P., Potter, D., Mistlin, A., Head, A., Milner, A., & Jeeves, M. (1985). Visual cells in the temporal cortex sensitive to face view and gaze direction. Proceedings of the Royal Society of London, B223, 293-317. Phillips, W., Baron-Cohen, S., & Rutter, M. (in press). Can children with autism understand intentions? . Pratt, C., & Bryant, P. (1990). Young children understand that looking leads to knowing (so long as they are looking into a single barrel). Child Development, 61, 973983. Reed, T., & Peterson, C. (1990). A comparative study of autistic subjects' performance at two levels of visual and cognitive perspective taking. Journal of Autism and Developmental Disorders, 20, 555-568. Russell, J. (1997a). How executive disorders can bring about an inadequate theory of mind. In J. Russell (Ed.), Autism as an executive disorder, . Oxford: Oxford University Press. Russell, J. (1997b). Introduction. In J. Russell (Ed.), Autism as an executive disorder, . Oxford: Oxford University Press. Scott, F., & Baron-Cohen, S. (1996). Imagining real and unreal objects: an investigation of imagination in autism. Journal of Cognitive Neuroscience, 8, 400-411. Shallice, T. (1988). From neuropsychology to mental structure. Cambridge: Cambridge University Press. Sodian, B., & Frith, U. (1992). Deception and sabotage in autistic, retarded, and normal children. Journal of Child Psychology and Psychiatry, 33, 591-606. Stone, V., Baron-Cohen, S., Young, A., & Calder, A. (1998). Patients with amygdalectomy show impairments in theory of mind : University of Cambridge. Surian, L., Baron-Cohen, S., & Van der Lely, H. (1996). Are children with autism deaf to Gricean Maxims? Cognitive Neuropsychiatry, 1, 55-72. Swettenham, J., Baron-Cohen, S., Gomez, J.-C., & Walsh, S. (1996). What's inside a person's head? Conceiving of the mind as a camera helps children with autism develop an alternative theory of mind. Cognitive Neuropsychiatry, 1, 73-88. Tager-Flusberg, H. (1992). Autistic children's talk about psychological states: deficits in the early acquisition of a theory of mind. Child Development, 63, 161-172. Tager-Flusberg, H. (1993). What language reveals about the understanding of minds in children with autism. In S. Baron-Cohen, H. Tager-Flusberg, & D. J. Cohen (Eds.), Understanding other minds: perspectives from autism, : Oxford University Press. Tager-Flusberg, H., Boshart, J., & Baron-Cohen, S. (in press). Reading the windows of the soul: evidence of domain specificity sparing in Williams syndrome. Journal of Cognitive Neuroscience. 24 Van der Lely, H. (1997). Language and cognitve development in a grammatical SLI boy: Modularity and Innateness. Journal of Neurolinguistics, 10, 75-107. Wing, L., & Gould, J. (1979). Severe impairments of social interaction and associated abnormalities in children: epidemiology and classification. Journal of Autism and Developmental Disorders, 9, 11-29. Yirmiya, N., Solomonica-Levi, D., & Shulman, C. (1996). The ability to manipulate behaviour and to understand manupulation of beliefs: A comparison of individuals with autism, mental retardation, and normal development. Developmental Psychology, 32, 62-69. 25